Case Discussion
Genevie Ramos Ombao February 28, 2012
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MR, 21 yo SNG
cc: irregular menses
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History of Present Illness
Menarche at 11 years old (10 years PTC)
Regular menstrual cycles every 28-30 days, 3 days duration,
consuming 4 pads per day, fully-soaked
13 years old (8 years PTC)
Started having irregular menses, going as long as 6 months in
between menses no consult was done or medications taken as she thought it was normal
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History of Present Illness
Interim
Patient continued to have irregular menstrual cycles , still no
consult done until
2010 (2 years PTC)
Consulted a local OBGYN for her complaint Pelvic ultrasound was done which allegedly showed an ovarian
cyst in the left
Patient was advised observation
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History of Present Illness
2011
Sought a 2nd opinion where TRS done allegedly still showed left
ovarian cyst
Patient was then given Lady pills which she took for 8 months
affording relief of irregular menses
Aug 2011: stopped taking the pills
Patient since has had no menses; pregnancy test done at home
was negative
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No hypertension, heart disease, thyroid disease, or
lung disease
(-) allergies No previous operations
Past Medical History
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Non-smoker Alcoholic beverage non-drinker
Personal and Social History
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No hypertension, diabetes, bronchial asthma,
thyroid disease
Family History
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Menstrual History
Menarche: 11 years old, regular; every 28-30 days,
lasts for 3 days, 4 pads per day, (-) pain
Subsequent Menses: irregular, lasts for 3 days, 4
pads per day, (-) pain
LMP: September 2011
PMP: August 2011
Menstrual History
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Single, nulligravid
OB History
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Contraception History
OCP use x 8 months
NO Pap smear
Gynecologic History
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General: no weight loss or gain, anorexia, fever Skin: no skin changes Eyes: no blurring of vision, redness, itchiness, discharge, pain Nose: No discharge, epistaxis, anosmia Mouth & Throat: No bleeding, circumoral cyanosis, hoarseness,
soreness, difficulty of swallowing
Pulmonary: no cough (-) hemoptysis, chest wall abnormalities
Review of Systems
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Heart: No palpitations, chest pain, chest heaviness Gastrointestinal: no changes in bowel habits Genitourinary: no hematuria, frequency, urgency, flank pain Vascular: no excessive bleeding, easy bruisability Neurologic: no headaches, no seizure episodes, weakness or numbness Endocrinologic : no tremors, no polyuira, no polydipsia , no polyphagia , no excessive growth of facial hair or baldness
Review of Systems
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BP: 120/80; Pulse rate: 81/minute, regular; Respiratory rate:
21/minute, regular; Temperature: 36.9 C; Weight: 71 kg; Height: 152 cm; BMI = 30 kg/m2
Moist skin, no active dermatosis
No facial involuntary movement, edema, masses
Pink palpebral conjunctivae, anicteric sclerae, patent external
auditory canal, non-congested turbinates, no nasal discharge, supple neck, no lymphadenopathies, no palpable anterior neck mass
Symmetrical chest expansions, clear breath sounds in all lung fields,
no retractions
Physical Examination
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Adynamic precordium, normal rate, regular rhythm,
S1>S2 apex, S2>S1 base, PMI at 5th LICS, no murmurs
Pulses full and equal Conscious, coherent, oriented to 3 spheres No sensorimotor deficits Deep tendon reflexes of upper and lower extremities: ++
Physical Examination
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Abdominal Exam
Abdomen globular, soft, non-tender, no palpable
masses
Physical Examination
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SUBJECTIVE
21 SNG irregular menses since 13 y/o Menarche at 11 with regular menses for 2 years
OBJECTIVE
BMI = 30 kg/m2
Salient Features
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Polycystic Ovarian Syndrome (PCOS)
endocrinopathy typified by oligo-ovulation or anovulation, signs of androgen excess, and multiple small ovarian cysts approximately 4 to 12 percent
most common endocrine disorder of reproductive-aged women and affects
PCOS Page 18
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Ovarian Hyperthecosis
condition characterized by nests of luteinized theca cells distributed throughout the ovarian stroma deepening of the voice
frank virilization signs such as clitoromegaly, temporal balding, and
HAIRAN Syndrome
hyperandrogenic-insulin resistant-acanthosis nigricans
may represent either a variant of PCOS or a distinct genetic syndrome
PCOS Page 19
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The underlying cause of PCOS is unknown
PCOS Page 20
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PCOS : Etiology
multifactorial
increased prevalence has been noted between affected individuals and
their sisters (32 to 66 percent) and mothers (24 to 52 percent)
studies of human ovarian theca cells have suggested dysregulation of the
CYP11a gene
encodes the cholesterol side-chain cleavage enzyme, the enzyme that performs the ratelimiting step in steroid biosynthesis
PCOS Page 21
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PCOS : Pathophysiology
Inappropriate
gonadotropin secretion
LH > FSH Increased levels
of LH in more than 50% of patients
PCOS Page 22
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PCOS : Pathophysiology
Inappropriate
gonadotropin secretion
LH > FSH Increased levels
of LH in more than 50% of patients
PCOS Page 23
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PCOS : Pathophysiology
Insulin resistance
Hyperinsulinemia
appears to be due
to a postbinding abnormality in insulin receptor-mediated signal transduction Long-term effects:
1. 2. 3.
Diabetes mellitus Cardiovascular disease Endometrial cancer
PCOS Page 24
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PCOS : Pathophysiology
Increased
androgen levels
insulin and LH
stimulate ovarian theca cell androgen production
Elevated free
testosterone 7080%; Elevated DHEAS 25-65%
PCOS Page 25
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PCOS : Pathophysiology
Decreased
SHBG
Produced in the
liver and binds to sex steroids
Supressed by
insulin and androgens
Increased
testosterone levels
PCOS Page 26
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PCOS : Pathophysiology
Anovulation
Mechanism is
unclear
Hypersecretion of LH Insulin-resistence
PCOS Page 27
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SIGNS AND SYMPTOMS
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Menstrual Dysfunction
Oligo- and amenorrhea
Chronic estrogen exposure
unopposed by the effects of postovulatory progesterone
Unstable thickened
endometrium unpredictable bleeding pattern
Irregular menstrual cycles
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Hyperandrogenism
typically manifested
clinically by hirsutism, acne, and/or androgenic alopecia
Different from virilization (
increased muscle mass, deepening of voice, clitoromegaly) !!!
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Insulin-Resistance
both lean and obese women
with PCOS have increased rates of insulin resistance and type 2 diabetes mellitus (DM) compared with weightmatched controls without PCOS (Dunaif, 1989, 1992).
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Obesity
Women with PCOS are more
likely to be obese, as reflected by an elevated body mass index (BMI) and waist:hip ratio (Talbott, 1995).
Apple shaped android or
central type of obesity
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Metabolic Syndrome and Cardiovascular Disease
characterized by insulin
resistance, obesity, atherogenic dyslipidemia, and hypertension
reported to be approximately
45 percent in women with PCOS compared with 4 percent in age-adjusted controls (Dokras, 2005).
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Endometrial Neoplasia
threefold increased risk of
endometrial cancer has been reported
long-term risks of chronic
anovulation, and neoplastic changes in the endometrium are felt to arise from chronic unopposed estrogen (Coulam, 1983).
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Infertility and Pregnancy Loss
results from anovulatory
cycles
Women with PCOS who
become pregnant are known to experience an increased rate (30 to 50 percent) of early miscarriage
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Other Pregnancy Complications
Women with PCOS have
a two- to threefold higher risk of gestational diabetes, pregnancyinduced hypertension, preterm birth, and perinatal mortality, unrelated to multifetal gestations
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DIAGNOSIS
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Polycystic ovarian syndrome is often referred to as a diagnosis of exclusion
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PCOS-mimickers: Thyroid Disease
also can manifest with
menstrual dysfunction and obesity
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Sonography
Histologically a polycystic ovary
(PCO) displays increases in volume, number of ripening and atretic follicles, cortical stromal thickness, and number of hilar cell nests
Sonographic criteria for
polycystic ovaries from the 2003 Rotterdam conference include 12 small cysts (2 to 9 mm in diameter) or an increased ovarian volume (>10 mL) or both
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Insulin Resistance
Although the consensus meeting
in Rotterdam suggested that tests of insulin resistance are not required to diagnose or treat PCOS, these tests are often used to evaluate glucose metabolism and impaired insulin secretion in these women
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TREATMENT
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The choice of treatment for each symptom of PCOS depends on a woman's goals and the severity of endocrine dysfunction.
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Observation
PCOS patients with fairly regular cycle intervals (8 to 12
menses per year) and mild hyperandrogenism may choose not to be treated
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Weight Loss
lifestyle changes focused on diet and exercise are
paramount to treatment at each stage of life
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Combination Oral Contraceptive Pills
first-line treatment
for menstrual irregularities
induce regular
menstrual cycles.
Decrease androgen
levels , increase SHBG levels
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Combination Oral Contraceptive Pills
How to?
if a woman's last menses was more
than 4 weeks prior, do a pregnancy test!
If negative, progesterone is given to produce a withdrawal bleed prior to COC initiation.
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Combination Oral Contraceptive Pills
How to?
Typical regimens include:
medroxyprogesterone acetate (MPA) (Provera, Pfizer, New York, NY), 10 mg orally daily for 10 days; MPA, 10 mg orally twice daily for 5 days; or micronized progesterone (Prometrium, Solvay Pharmaceuticals, Marietta, GA), 200 mg orally daily for 10 days.
Lady Pills : Levonorgestrel 150
mcg, ethinyl estradiol 30 mcg
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Insulin-Sensitizing Agents
improves peripheral insulin sensitivity
by reducing hepatic glucose production and increasing target tissue sensitivity to insulin
decreases androgens in both lean and
obese women, leading to increased rates of spontaneous ovulation
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PROGNOSIS
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PCOS is a chronic condition. There is no cure. Thus, management options are targeted at alleviating the signs and symptoms to reduce morbidity. Another goal of treatment is to prevent the development of complications
- BMJ, 2011
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PCOS Prognosis
therapy is generally continued throughout the
reproductive years. If treatments are stopped during that time, symptoms generally recur
Once a woman with PCOS reaches
menopause, hyperandrogenic manifestations may improve as ovarian function declines, allowing withdrawal of therapies directed against hyperandrogenism
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Monitoring
Patients should be evaluated every 3 months for
treatment response and development of any adverse effects. Once stable, monitoring is every 6 months.
Combination therapy may be required to achieve results
in ameliorating hyperandrogenism.
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Thank you
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